A 10-15 year old, about 450 kg, Standardbred mare, 38 days in foal, was hospitalized because of an acute onset of abnormal behavior. The mare was noticed to be off feed and within 24 hours began showing signs of a central nervous system (CNS) disturbance: circling, wall biting, and head pressing. On initial exam the mare had hypomotile gastrointestinal (GI) sounds, abrasions over the eyes and nose, a swollen muzzle, and slight icterus. Abnormal CNS findings were depression, head pressing, a slow menace, a slow direct pupillary light reflex, and an unsteady gait. A complete blood count (CBC) revealed hemoconcentration (PVC, 44%; normal: 31-43.7%) and a leukocytosis (23,700 cell/ul; normal: 5,500-12,000 cells/ul) with neutropilia (19,400 cells/ul; normal: 2,600-6,500 cells/ul), a slight left shift (900 band cells/ul; normal: 0 band cells/ul), and monocytosis (1,700 cells/ul: normal: 0-400 cells/ul). The plasma was moderately icteric. Serum biochemical analysis revealed hypochloremia (94 mEq/L; normal: 97-107 mEq/L), hyperglycemia (129 mg/dl; normal: 73-112 mg/dl), and increased aspartate aminotransferase (AST; 2135 U/L; normal: 193-509 U/L), gammaglutamyl transferase (GGT; 206 U/L; normal: 10-59 U/L), and total bilirubin (BR) (10.9 mg/dl; normal: 0.3-3-5 mg/dl). The mare had a metabolic acidosis (bicarbonate = 21 mEq/L; normal: 24-30 mEq/L). The mare originally referred to the teaching hospital as a rabies suspect, however, the elevated liver enzymes made a primary liver disease more likely, and fluid therapy to correct dehydration and to decrease possible cerebral edema was initiated. The mare was given intravenous (IV) lactated ringer’s solution (LRS) containing 20 mEq/L potassium chloride (KCl) at 3 L/hr. In addition, the mare received 500 g dimethyl sulfoxide in 4 liters of LRS containing 20 mEq/L KCl. Intravenous antibiotic therapy was initiated (15 g Tribrissen IV, q 12 h). The mare was offered hay and water, ad lib.